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Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers

ABSTRACT: Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers

PROVIDER: PRJNA427593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6423120_1.fastq.gz	Fastqsanger.gz
	SRR6423120_2.fastq.gz	Fastqsanger.gz
	SRR6423130_1.fastq.gz	Fastqsanger.gz
	SRR6423130_2.fastq.gz	Fastqsanger.gz
	SRR6423140_1.fastq.gz	Fastqsanger.gz

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Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Livers

Project description:Purpose: A1CF is an RNA binding protein that has not been extensively studied on a transcriptome-wide scale. Here we profile the livers of wild-type and A1cf knockout mice to detect differences in gene expression. Methods: mRNA profiles of 6-8 week old wild-type and A1cf knockout mice were generated by deep sequencing using Illumina HiSeq 2500. Reads that passed quality filters were aligned to mm10 genome and analyzed for differential expression using CuffDiff2 and DESeq2. Results: We mapped reads to the mm10 genome and found a subset of fewer than 500 differentially expressed genes in A1CF deficiency. Conclusions: Our study represents the first transcriptomic profiling of A1CF deficiency in the liver.

2019-10-31 | GSE108547 | GEO

Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Whole Kidneys

Project description:Purpose: A1CF is an RNA binding protein that has not been extensively studied on a transcriptome-wide scale. Here we profile the whole kidneys of wild-type and A1cf knockout mice to detect differences in gene expression. Methods: mRNA profiles of 6-8 week old wild-type and A1cf knockout mice were generated by deep sequencing using Illumina HiSeq 2500. Reads that passed quality filters were aligned to mm10 genome and analyzed for differential expression using CuffDiff2 and DESeq2. Results: We mapped reads to the mm10 genome and found a subset of fewer than 500 differentially expressed genes in A1CF deficiency. Conclusions: Our study represents the first transcriptomic profiling of A1CF deficiency in the kidney.

2019-07-01 | GSE108548 | GEO

Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice

Project description:Rationale: RNA binding protein Apobec1 Complementation Factor (A1CF) regulates posttranscriptional ApoB mRNA editing but the range of RNA targets and long-term impact of altered A1CF expression on liver function are unknown. Objective: We studied hepatocyte-specific A1cf transgenic (A1cf +/Tg), A1cf+/Tg Apobec1– /– and A1cf –/– mice fed chow or high fat/high fructose diets using RNA-Seq, RNA-CLIP Seq and tissue microarrays from human hepatocellular cancer (HCC). Findings: A1cf +/Tg mice exhibited increased hepatic proliferation and steatosis, with increased lipogenic gene expression (Mogat1, Mogat2, Cidea, Cd36) associated with shifts in polysomal RNA distribution. Aged A1cf +/Tg mice developed spontaneous fibrosis, dysplasia and HCC, which was accelerated on a high fat/fructose diet and independent of Apobec1. RNA-Seq revealed increased expression of mRNAs involved in oxidative stress (Gstm3, Gpx3, Cbr3), inflammatory response (Il19, Cxcl14, Tnfα, Ly6c), extracellular matrix organization (Mmp2, Col1a1, Col4a1), proliferation (Kif20a, Mcm2, Mcm4, Mcm6) with a subset of mRNAs (including Sox4, Sox9, Cdh1) identified in RNA CLIP-Seq. Increased A1CF expression in human HCC correlated with advanced fibrosis and with reduced survival in a subset with nonalcoholic fatty liver disease. Conclusions: Hepatic A1CF overexpression selectively alters polysomal distribution and mRNA expression, promoting lipogenic, proliferative and inflammatory pathways leading to HCC.

2020-09-01 | GSE157233 | GEO

Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice

Project description:Comparative gene expression profiling in livers of A1cf-transgenic, A1cf-knockout, and wild-type mice

| PRJNA660481 | ENA

Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Whole Kidneys

Project description:Transcriptome Profiling of Wild-type vs. A1CF -/- Mouse Whole Kidneys

| PRJNA427594 | ENA

Comparative gene expression profiling in livers of A1cf-transgenic and wild-type mice

2020-09-05 | GSE157516 | GEO

Comparative gene expression profiling in livers of A1cf-transgenic and wild-type mice

Project description:Comparative gene expression profiling in livers of A1cf-transgenic and wild-type mice

| PRJNA661555 | ENA

Interactomics Analyses of Wild-type and Mutant A1CF Reveal Diverged Functions in Regulating Cellular Lipid Metabolism

Project description:Population genetic studies highlight a missense variant (G398S) of A1CF that is strongly associated with higher levels of blood triglycerides (TGs) and total cholesterol (TC). Functional analyses suggest that the mutation accelerates the secretion of very low-density lipoprotein (VLDL) from the livers by an unknown mechanism. Here, we used multi-omics approaches to interrogate the functional difference between the WT and mutant A1CF. Using metabolomics analyses, we captured the cellular lipid metabolite changes induced by the transient expression of the proteins, confirming that the mutant A1CF is able to relieve the TG accumulation induced by WT A1CF. Using a proteomics approach, we obtained the interactomic data of WT and mutant A1CF. Networking analyses show that WT A1CF interacts with three functional protein groups, RNA/mRNA processing, cytosolic translation and, surprisingly, mitochondrial translation. The mutation diminishes these interactions, especially with the group of mitochondrial translation. Differential analyses show that the WT A1CF-interacting proteins most significantly different from the mutant are those for mitochondrial translation, whereas the most significant interacting proteins with the mutant are those for cytoskeleton and vesicle-mediated transport. RNA-seq analyses validate that the mutant, but not the WT, A1CF increases the expression of the genes responsible for cellular transport processes. On the contrary, WT A1CF affected the expression of mitochondrial matrix proteins and increased cell oxygen consumption. Thus, our studies confirm the previous hypothesis that A1CF plays broader roles in regulating gene expression. The interactions of the mutant A1CF with the vesicle-mediated transport machinery provide mechanistic insight in understanding the increased VLDL secretion in the A1CF mutation carriers.

2022-06-30 | GSE152807 | GEO

C57BL6/J livers exposed to low fat and high fat diet, wild-type vs Cyp1b1 null

Project description:Investigating the transcriptional changes in mouse livers exposed to low and high fat diets for 11 weeks. Determine what gene changes in the Cyp1b1 null livers may be contributing to prevention of increased adiposity when givin a high fat diet. Three Comparison experiment. Comparing wild-type low fat vs Cyp1b1 null low fat, wild-type high fat vs Cyp1b1 null high fat and low fat vs high in wild-type mice. Sample size is 3 per group. Limma analysis data provided in Series supplementary file (Normalized log2 ratio of (Cy3/Cy5) representing test group/control group).

2014-01-09 | E-GEOD-53910 | biostudies-arrayexpress

scRNAseq from Li-TSC1KORagAGTP and wild-type livers

Project description:scRNAseq from Li-TSC1KORagAGTP and wild-type livers

| PRJNA956282 | ENA